Muscle from humans and animals with myotonia congenita has physiological, structural and biochemical alterations which transcend the loss of CLC-1 channels, including hypertrophy (goats, most humans) or atrophy (mice), alterations in fiber type composition (in particular loss of type IIB fibers, seen in most species with myotonia congenita), and altered amounts of parvalbumin [1,5,7,9,11-13,17,18]. The gene discussed is PVALB; the disease is Thomsen and Becker disease.